Abstract：The objective of this study was to investigate the protective effect and mechanism of angiotensin converting enzyme 2(ACE2) on renal oxidative stress injury induced by high glucose. The rats(Rattus norregicus) model of renal oxidative stress injury was established by intraperitoneal injection of streptozotocin(STZ) solution, and treated by subcutaneous injection of insulin once a day(1 mL (3.7×10-5 mol/L)). After 30 days, all the rats were decapitated and the serum and kidney tissue were collected. The contents of advanced glycation end products (AGEs), malondialdehyde(MDA), superoxide dismutase(SOD), angiotensinⅡ(AngⅡ), angiotensin1-7(Ang1-7) in serum and the mRNA levels of ACE2 and Mas receptor in kidneys were measured. Compared with control group, the contents of AGEs, MDA and AngII in serum of high glucose rats were significantly increased(P<0.01), and the levels of SOD and Ang1-7 in serum were significantly decreased(P<0.01). The mRNA expression of ACE2 in kidneys was obviously reduced(P<0.01), while the mRNA expression of Mas was obviously raised(P<0.01). After insulin treatment, the contents of AGEs and MDA in serum were obviously reduced(P<0.01); the activity of SOD in serum was significantly raised(P<0.01); the level of AngII in serum was significantly decreased(P<0.05) while the concentration of Ang1-7 in serum was significantly increased(P<0.05). The mRNA expression levels of ACE2 and Mas receptor in kidneys were significantly increased(P<0.01). Exparemental results suggest that ACE2 plays an important role on the renal oxidative stress injury induced by high glucose and the mechanism may be that the activation of the ACE2-Ang1-7-Mas axis reduces the effect of AngⅡ.
